Evidence map›Paper›PMID 30382937›Full record

ArticleeLife2018

Deletion of KCNQ2/3 potassium channels from PV+ interneurons leads to homeostatic potentiation of excitatory transmission.

Heun Soh, Suhyeorn Park, Kali Ryan, Kristen Springer, Atul Maheshwari, Anastasios V Tzingounis

Open access · goldAbstract read
In one paragraph

Article in eLife, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.8field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

36 citing papers in PubMed, 63 citations in OpenAlex.

  1. Review
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  7. Heterozygous expression of abioRxiv : the preprint server for biology · 2024
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  8. Plural molecular and cellular mechanisms of pore domainbioRxiv : the preprint server for biology · 2024
    Article
  9. Article
  10. KCNQ2/3 Gain-of-Function Variants and Cell Excitability: Differential Effects in CA1 versus L2/3 Pyramidal Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  11. A Role for KCNQ Channels on Cell Type-Specific Plasticity in Mouse Auditory Cortex after Peripheral Damage.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  12. Article
  13. Review
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  18. Article
  19. Autism-associated mutations in KProceedings of the National Academy of Sciences of the United States of America · 2021
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Heun Soh *Department of Physiology and Neurobiology, University of Connecticut, Connecticut, United States.
Suhyeorn Park *Department of Neurology, Baylor College of Medicine, Texas, United States.
Kali RyanDepartment of Physiology and Neurobiology, University of Connecticut, Connecticut, United States.
Kristen SpringerDepartment of Physiology and Neurobiology, University of Connecticut, Connecticut, United States.
Atul MaheshwariDepartment of Neurology, Baylor College of Medicine, Texas, United States.ORCID 0000-0003-3045-7901
Anastasios V TzingounisDepartment of Physiology and Neurobiology, University of Connecticut, Connecticut, United States.ORCID 0000-0002-4605-3437
University of Connecticut · USBaylor College of Medicine · US

Funding

Role of KCNQ2 Channels in Control of BreathingR01HL137094 · NHLBI · UNIVERSITY OF CONNECTICUT STORRS · PI MULKEY, DANIEL K, TZINGOUNIS, ANASTASIOS · 2018 to 2025
$4.1M
KCNQ2/3 channels and interneuron physiologyR01NS101596 · NINDS · UNIVERSITY OF CONNECTICUT STORRS · PI TZINGOUNIS, ANASTASIOS · 2017 to 2021
$1.7M
Cellular physiology of epilepsy-associated KCNQ2 channelsR01NS073981 · NINDS · UNIVERSITY OF CONNECTICUT STORRS · PI TZINGOUNIS, ANASTASIOS · 2011 to 2015
$1.6M
Cellular and Network Basis of Anti-Epileptic Drug ResponseK08NS096029 · NINDS · BAYLOR COLLEGE OF MEDICINE · PI MAHESHWARI, ATUL · 2016 to 2020
$943k
CELLULAR PHYSIOLOGY OF EPILEPSY-ASSOCIATED KCNQ2 and KCNQ3 CHANNELSR56NS073981 · NINDS · UNIVERSITY OF CONNECTICUT STORRS · PI TZINGOUNIS, ANASTASIOS · 2016 to 2016
$388k
NHLBI NIH HHS R01 HL137094NIH HHS NS073981NIH HHS NS096029NIH HHS NS101596NINDS NIH HHS K08 NS096029NINDS NIH HHS R01 NS073981NINDS NIH HHS R01 NS101596NINDS NIH HHS R56 NS073981
6 · The paper itself

Abstract

KCNQ2/3 channels, ubiquitously expressed neuronal potassium channels, have emerged as indispensable regulators of brain network activity. Despite their critical role in brain homeostasis, the mechanisms by which KCNQ2/3 dysfunction lead to hypersychrony are not fully known. Here, we show that deletion of KCNQ2/3 channels changed PV

Indexed as

Gene DeletionHomeostasisSynaptic TransmissionAnimalsFemaleInterneuronsKCNQ2 Potassium ChannelKCNQ3 Potassium ChannelMaleMicePotassium Channel BlockersPyramidal CellsKCNQ2 Potassium ChannelKCNQ3 Potassium ChannelPotassium Channel BlockersepilepsyinterneuronsKCNQ2KCNQ3mouseneuroscienceparvalbuminpotassium channelsseizure

Identifiers

PMID30382937
PMCPMC6211828
OpenAlexW2899372763

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.